PRESENTED BY

• Annisa Janettia (14700102)• I Made Ngurah Yogi Wisnu (14700114)• Anggun Eka Pratiwi (14700126)• I Gede Kisswa Gautama (14700138)• Ni Putu Diah Kumala Dewi (14700150)• Puji Oktavi Sumantiasa (14700162)• Kumala Sinta Dhamayanti (14700174)

GASTRITIS

DEFINITIONGastritis describes a group of conditions with one thing in common:

inflammation of the lining of the stomach. The inflammation of gastritis is most often the result of infection with the same bacterium that causes most stomach ulcers. Injury, regular use of certain pain relievers and drinking too much alcohol also can contribute to gastritis

COMPLICATIONS

• Left untreated, gastritis may lead to stomach ulcers and stomach bleeding. Rarely, some forms of chronic gastritis may increase your risk of stomach cancer, especially if you have extensive thinning of the stomach lining and changes in the lining's cells.

• Tell your doctor if your signs and symptoms aren't improving despite treatment for gastritis.

RISK FACTOR

• Bacterial infection. Although infection with Helicobacter pylori is among the most common worldwide human infections, only some infected people develop gastritis or a similar stomach disorder.

• Regular use of pain relievers. Common pain relievers — such as aspirin, ibuprofen (Advil, Motrin IB, others) and naproxen (Aleve, Anaprox) — can cause both acute gastritis and chronic gastritis.

• Excessive alcohol use. Alcohol can irritate your stomach lining, which makes your stomach more likely to be harmed by digestive juices

• Older age. Older adults have an increased risk of gastritis because the stomach lining tends to thin with age and because older adults are more likely to have H.

• Stress. Severe stress due to major surgery, injury, burns or severe infections can cause acute gastritis.

• Other diseases and conditions. Gastritis may be associated with other medical conditions, including HIV/AIDS, Crohn's disease and parasitic infections.

Symptoms of GASTRITIS

The signs and symptoms of gastritis include:• Gnawing or burning ache or pain (indigestion) in your

upper abdomen that may become either worse or better with eating

• Nausea• Vomiting• A feeling of fullness in your upper abdomen after eating• Gastritis doesn't always cause signs and symptoms.

CAUSES

• Gastritis is an inflammation of the stomach lining. Weaknesses in the mucus-lined barrier that protects your stomach wall allow your digestive juices to damage and inflame your stomach lining. A number of diseases and conditions can increase your risk of gastritis.

• Gastritis can develop suddenly (acute gastritis) or gradually and last for an extended period (chronic gastritis)

Diagnosing GASTRITIS

• Although your doctor is likely to suspect gastritis after talking to you about your medical history and performing an exam, you may also have tests to pinpoint the exact cause. Tests may include:

• Tests for H. pylori. Your doctor may recommend tests to determine whether you have the bacterium H. pylori. Which type of test you undergo depends on your situation. H. pylori may be detected in a blood test, in a stool test or by a breath test. For the breath test, you drink a small glass of clear, tasteless liquid that contains radioactive carbon. H. pylori bacteria break down the test liquid in your stomach. Later, you blow into a bag, which is then sealed. If you're infected with H. pylori, your breath sample will contain the radioactive carbon.

• Using a scope to examine your upper digestive system (endoscopy). During endoscopy, your doctor passes a flexible tube equipped with a lens (endoscope) down your throat and into your esophagus, stomach and small intestine. Using the endoscope, your doctor looks for signs of inflammation. If a suspicious area is found, your doctor may remove small tissue samples (biopsy) for laboratory examination. A biopsy can also identify the presence of H. pylori in your stomach lining.

• X-ray of your upper digestive system. Sometimes called a barium swallow or upper gastrointestinal series, this series of X-rays creates images of your esophagus, stomach and small intestine to look for abnormalities. To make the ulcer more visible, you swallow a white, metallic liquid (containing barium) that coats your digestive tract.

TREATMENT

• There is no specific medicine to treat dengue infection. If you think you may have dengue fever, you should use pain relievers with acetaminophen and avoid medicines with aspirin, which could worsen bleeding. You should also rest, drink plenty of fluids, and see your doctor. If you start to feel worse in the first 24 hours after your fever goes down, you should get to a hospital immediately to be checked for complications.

Preventing GASTRITIS

• Preventing H. pylori infection• It's not clear how H. pylori spreads, but there's some

evidence that it could be transmitted from person to person or through contaminated food and water. You can take steps to protect yourself from infections, such as H. pylori, by frequently washing your hands with soap and water and by eating foods that have been cooked completely

LIFESTYLE

• Eat smaller, more-frequent meals• Avoid irritating foods• Avoid alcohol• Consider switching pain relievers• Manage stress

UPDATING JOURNALABSTRACT

Disease due to the gastric pathogen Helicobacter pylori varies in severity from asymptomatic to peptic ulcer disease and cancer. Accumulating evidence suggests that one source of this variation is an abnormal host response. The goal of this study was to use a mouse model of H. pylori gastritis to investigate the roles of regulatory T cells (Treg) as well as proinflammatory T cells (Th1 and Th17) in gastritis, gastric T cell engraftment, and gastric cytokine production. Our results support published data indicating that severe gastritis in T cell recipient mice is due to failure of Treg engraftment, that Treg ameliorate gastritis, and that the proinflammatory response is attributable to interactions between several cell subsets and cytokines. We confirmed that gamma interferon (IFN-γ) is essential for induction of gastritis but showed that IFN-γ-producing CD4 T cells are not necessary. Interleukin 17A (IL-17A) also contributed to gastritis, but to a lesser extent than IFN-γ. Tumor necrosis factor alpha (TNF-α) and IL-17F were also elevated in association with disease. These results indicate that while H. pylori-specific CD4+ T cells and IFN-γ are both essential for induction of gastritis due to H. pylori, IFN-γ production by T cells is not essential. It is likely that other proinflammatory cytokines, such as IL-17F and TNF-α, shown to be elevated in this model, also contribute to the induction of disease. We suggest that gastritis due to H. pylori is associated with loss of immunoregulation and alteration of several cytokines and cell subsets and cannot be attributed to a single immune pathway.Disease due to the gastric pathogen Helicobacter pylori varies in severity from asymptomatic to peptic ulcer disease and cancer. Accumulating evidence suggests that one source of this variation is an abnormal host response. The goal of this study was to use a mouse model of H. pylori gastritis to investigate the roles of regulatory T cells (Treg) as well as proinflammatory T cells (Th1 and Th17) in gastritis, gastric T cell engraftment, and gastric cytokine production. Our results support published data indicating that severe gastritis in T cell recipient mice is due to failure of Treg engraftment, that Treg ameliorate gastritis, and that the proinflammatory response is attributable to interactions between several cell subsets and cytokines. We confirmed that gamma interferon (IFN-γ) is essential for induction of gastritis but showed that IFN-γ-producing CD4 T cells are not necessary. Interleukin 17A (IL-17A) also contributed to gastritis, but to a lesser extent than IFN-γ. Tumor necrosis factor alpha (TNF-α) and IL-17F were also elevated in association with disease. These results indicate that while H. pylori-specific CD4+ T cells and IFN-γ are both essential for induction of gastritis due to H. pylori, IFN-γ production by T cells is not essential. It is likely that other proinflammatory cytokines, such as IL-17F and TNF-α, shown to be elevated in this model, also contribute to the induction of disease. We suggest that gastritis due to H. pylori is associated with loss of immunoregulation and alteration of several cytokines and cell subsets and cannot be attributed to a single immune pathway.

introdruction

• In the 30 years since Warren and Marshall first made the association between Helicobacter pylori infection and peptic ulcer disease (1, 2), considerable progress has been made in understanding the pathogenesis of disease due to this organism. Several important virulence factors have been identified (3–5) (for reviews, see references 6 to8), and the roles of the host immune and inflammatory responses have been described in detail (for recent reviews, see references 8 to 10). We (11) and others (12) have shown that CD4 T cells are essential for induction of disease in animal models, and many laboratories have shown that proinflammatory cytokines are present in association with infection in both humans and experimental animals (13–16). Specifically, gamma interferon (IFN-γ) is well established as important in the pathogenesis of disease (14, 15), and H. pylori is generally considered to induce a Th1-biased host response, although recent findings suggest that other proinflammatory cytokines, such as interleukin 17 (IL-17) and tumor necrosis factor alpha (TNF-α), are also important (for a review, see reference10).

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